摘要:

This experiment was conducted to develop an understanding of mechanisms responsible for effects of a compensatory (stair‐step) growth pattern on the expression of milk protein genes and mammary differentiation. One hundred thirty weanling female rats were randomly assigned to either a control or a test group (compensatory growth). Early lactating mammary tissues from the compensatory growth group showed an increase in the RNA:DNA ratio, protein:DNA ratio, DNA, RNA, and protein while exhibiting a decrease in the lipid content as compared with those of the control group (2.2, 1.6, 1.7, 3.8, 2.8, and 0.5 times, respectively). Mammary tissues from the compensatory growth group contained about 1.1‐ to 1.4‐fold more total cytoplasmic mRNA for caseins and whey acidic protein than those of the control group. The compensatory growth pattern increased β‐casein mRNA accumulation, milk protein secretion, and amino acid uptake in mammary acinar culture (1.3, 1.3, and 1.1 times, respectively) compared with those of the control group. These results indicate that the compensatory growth pattern increases milk protein mRNA transcripts and may contribute to an increase in the functional activity of the mammary gland.—Park, C. S.; Choi, Y. J.; Keller, W. L.; Harrold, R. L. Effects of compensatory growth on milk protein gene expression and mammary differentiation.FASEB J.2: 2619‐2624; 1988.

ISSN:0892-6638    

DOI:10.1096/fasebj.2.10.2454864

出版商:Wiley    

年代:1988

数据来源: WILEY

摘要:

Sodium ion and chloride transport was studied in vitro in small intestinal and colonic tissue from patients with cystic fibrosis (CF) and from non‐CF control subjects matched as to age and sex. Normal histological appearance and substantial response to mucosal glucose (5 mM, ileum) or mucosal amiloride (10−5M, colon) indicated normal tissue viability in both control and CF tissues. Electroneutral NaCl absorption was demonstrated in the small intestine of control subjects and CF patients. Small intestinal and colonic tissues of control subjects responded to four secretagogues (theophylline, 5 mM; prostaglandin E2, 10−6M; calcium ionophore (A23187), 10−5M; bethanechol, 5 × 10−5M), with electrogenic chloride secretion. The tissues of CF patients, however, did not respond to any of the test secretagogues. These studies demonstrate that an abnormality in chloride transport is present in the small intestinal and colonic epithelia of CF patients. Unlike airway epithelia, which secrete chloride in response to Ca ionophore, the intestinal epithelia of CF patients do not respond to either cAMP‐ or Ca‐mediated secretagogues. This abnormality in intestinal electrolyte transport may play a role in the pathogenesis of meconium impactions in CF patients.— Berschneider, H. M.; Knowles, M. R.; Azizkhan, R. G.; Boucher, R. C.; Tobey, N. A.; Orlando, R. C.; Powell, D. W. Altered intestinal chloride transport in cystic fibrosis.FASEB J.2: 2625‐2629; 1988.

ISSN:0892-6638    

DOI:10.1096/fasebj.2.10.2838365

出版商:Wiley    

年代:1988

数据来源: WILEY

ISSN:0892-6638    

DOI:10.1096/fasebj.2.10.3384241

出版商:Wiley    

年代:1988

数据来源: WILEY